Sympathetic neural hyperactivity and its normalization following unstable angina and acute myocardial infarction

Abstract

Impaired autonomic function occurs after AMI (acute myocardial infarction) and UA (unstable angina), which may be important prognostically. However, the pattern of sympathetic nerve hyperactivity has been investigated only after AMI. We aimed to quantify central sympathetic output to the periphery in patients with UA, investigate its progress over time relative to that after uncomplicated AMI and to explore the mechanisms involved. Muscle sympathetic nerve activity (MSNA) assessed from multiunit discharges and from single units (s-MSNA) was obtained in matched patients with UA ( n =9), AMI ( n =14) and stable CAD (coronary artery disease, n =11), patients with chest pain in which AMI was excluded (NMI, n =9) and normal controls (NCs, n =14). Measurements were obtained 2-4 days after UA or AMI, and repeated at 3 monthly intervals until they returned to normal levels. The respective MSNA and s-MSNA early after UA (72+/-4.0 bursts/100 beats and 78+/-4.2 impulses/100 beats respectively) were less than those after AMI (83+/-4.4 bursts/100 beats and 93+/-5.5 impulses/100 beats respectively). Relative to the control groups of NCs (51+/-2.7 bursts/100 beats and 58+/-3.4 impulses/100 beats respectively) and patients with CAD (54+/-3.7 bursts/100 beats and 58+/-3.9 impulses/100 beats respectively) and NMI (52+/-4.5 bursts/100 beats and 59+/-4.9 impulses/100 beats respectively), values returned to normal after 6 months in UA (55+/-5.0 bursts/100 beats and 62+/-5.5 impulses/100 beats respectively) and 9 months after AMI (60+/-3.8 bursts/100 beats and 66+/-4.2 impulses/100 beats respectively). In conclusion, both UA and AMI result in sympathetic hyper-activity, although this is of smaller magnitude in UA and is less protracted than in AMI. It is suggested that this hyperactivity is related to the degree of left ventricular dysfunction and reflexes.

Sleep Disordered Breathing in Patients with Acute Coronary Syndromes

“…However, in such cases there is a tendency for central respiratory events to occur, which did not appear in our results since patients with cardiac failure were excluded. Another explanation may be inflammatory changes and sympathetic neural hyperactivity associated with ACS, 33 which could lead to destabilization of ventilatory control, affecting upper airway patency as well as chest wall muscles. 34 Considering that smoking is a predisposing factor for OSAHS, 35 an apparent explanation for the observed decrease of AHI 6 months later is that 12 of 16 current smokers in our study stopped smoking, with most of them included in the group of the 22 with decreased AHI 6 months later.…”

Improving Myocardial Perfusion by Percutaneous Coronary Intervention Reduces Central Sympathetic Activity in Stable Angina

“…Myocardial ischemia is closely related to an increase in central sympathetic activity. 2,15 Sympathetic afferents residing in the myocardial wall are triggered by a number of substances released during ischemia. 3 -5 When afferent stimulation is sufficient, a reflex mechanism ensues, increasing central sympathetic outflow, with the degree of ischemia being correlated with the degree of central sympathoexcitation.…”

“…3 -5 When afferent stimulation is sufficient, a reflex mechanism ensues, increasing central sympathetic outflow, with the degree of ischemia being correlated with the degree of central sympathoexcitation. 2 This state of increased sympathetic tone seems to persist beyond the ischemic event. 1 To our knowledge, there are no studies that have shown that reversal of ischemia by PCI reduces central sympathetic tone.…”

“…Baseline MSNA levels were similar to those of patients with acute onset unstable angina (72 ± 4 bursts/100 beats vs 78 ± 4 bursts/100 beats for unstable angina) and clearly increased compared to patients with asymptomatic stable CAD (54 ± 4 bursts/100 beats). 2 This strongly suggests that ischemia is an important determinant of sustained sympathetic stimulation. Improving myocardial perfusion by successful PCI should therefore improve myocardial oxygenation, reduce afferent stimulation, and subsequently decrease central sympathetic outflow.The present study does show a significantreduction in central sympathetic nerve traffic after PCI.…”

“…1,2 The most likely explanation is stimulation of sympathetic afferents in the myocardial wall due to ischemia-induced release of a number of afferentstimulating substances. 3,4 If the ischemic stimulus is strong enough, a reflex increase in central sympathetic output occurs, despite current pharmacological interventions.…”